The Surgical clinics of North America
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Surg. Clin. North Am. · Aug 1985
ReviewMyocardial function in the critically ill: factors influencing left and right ventricular performance in patients with sepsis and trauma.
Myocardial performance in critically ill patients is primarily responsive to the need to supply O2 to the periphery. An increase in CO is the common finding in an acute illness characterized by an increase in systemic VO2 (for example, sepsis and trauma), since acute variations in flow are the most efficacious mode of augmenting systemic O2t to match the VO2. The lower systemic VO2 of a patient with an acute cardiac illness explains why the CO in this disease is not as elevated as that found in the acutely ill patient with sepsis or trauma. ⋯ Vasodilators may be used to increase CO by reducing impedance to ventricular ejection; they may also improve LV compliance, thereby allowing the administration of more fluid (that is, increasing preload) without an untoward rise in the PCWP. If vasodilators are without effect or are potentially dangerous because of concomitant hypotension, inotropic support to increase O2t is required. A brief summary of interventional pharmacologic support in acute illness is depicted in Figure 8.
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Adult respiratory distress syndrome remains one of the most lethal conditions treated in surgical and medical intensive care units. Mortality rates of 50 per cent are still reported in recent reviews. Many risk factors are linked with an increased incidence of ARDS, but sepsis and direct pulmonary injury from aspiration, pulmonary contusion, and other forms of trauma are the most commonly associated risk factors. ⋯ Therapy should be started at this time and maintained while the etiologic factors are identified and treated. Minimal ventilatory support should be continued until the primary diseases have resolved and the multisystem impact of the critical illness has lessened. Weaning from inspiratory (IMV) support, manipulation of expiratory pressures (PEEP), and airway control should then be more easily accomplished and more successful in practice.
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Surg. Clin. North Am. · Aug 1985
Review Clinical TrialTherapy of critically ill postoperative patients based on outcome prediction and prospective clinical trials.
An objective physiologic approach to therapy of high-risk postoperative patients was developed using survival as the criterion to determine the relative importance of variables and optimal goals for these variables. A protocol, based on a branch chain decision tree, also was developed from outcome data. When tested prospectively against the standard of care, this protocol markedly reduced mortality and morbidity.
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From the foregoing accounts of preoperative assessment of myocardial performance, as well as preload and afterload status it is clear that the proper anesthesia techniques and agents can be selected. Physiologically optimal adjustments of preload, afterload, and myocardial function can be attained by the appropriate, harmonious selection of anesthesia technique and vasoactive drugs made on the basis of close hemodynamic monitoring preoperatively, intraoperatively, and in the immediate postoperative period.
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Surg. Clin. North Am. · Aug 1985
Review Comparative StudyControversies in the pathophysiology and fluid management of postoperative adult respiratory distress syndrome.
Physiologic changes that lead to the development of ARDS begin with the precipitating shock syndrome. Hypovolemia, pulmonary vasoconstriction, reduced myocardial performance, and diminished O2 transport typically precede the development of clinical ARDS after hemorrhage, trauma, postoperative conditions, and sepsis. Since shock lung is a complication of shock, it is not surprising that the antecedent clinical and physiologic events that characterize the shock state may be determinants of both the genesis and the outcome of ARDS. ⋯ They are uneven ventilation throughout the lung; redistribution of regional pulmonary blood flow between zones due to gravity; nonuniform pulmonary blood flow between individual metarteriolar-capillary networks because of local vasoconstriction; uneven systemic blood flow between organs; irregular systemic blood flow at the microcirculatory level, producing inadequate nutritional flow to the tissues; and redistribution of body water, leading particularly to fluid accumulation in the extracellular compartment, with expanded interstitial space and contracted plasma volume (hypovolemia). Pathogenic roles have been implicated for capillary leak, surfactant synthesis, erythrocyte and platelet aggregation, leukocyte margination in the pulmonary circulation, complement and kinin cascades, neurohumoral responses, histamine, serotonin, vasoactive peptides, and the metabolic products of arachidonic acid breakdown in pulmonary vessels. However, these potential pathogenic influences have yet to be described in terms of their temporal relationships to the natural physiologic history of ARDS; nor have their roles been evaluated in terms of mechanistic interrelationships.(ABSTRACT TRUNCATED AT 400 WORDS)